机构地区:[1]解放军总医院第一医学中心内分泌科,北京100853
出 处:《中华糖尿病杂志》2025年第1期153-161,共9页CHINESE JOURNAL OF DIABETES MELLITUS
基 金:国家重点研发计划(2021YFC2701901)。
摘 要:目的探讨Gitelman综合征(GS)患者糖代谢异常的影响因素。方法该研究为病例对照研究。选取2013年1月至2023年9月于解放军总医院第一医学中心内分泌科住院治疗的GS患者和无功能性肾上腺意外瘤(NFAI)患者为研究对象。收集研究对象的空腹胰岛素、空腹血糖、血钾、血镁、身高、体重,并行口服葡萄糖耐量试验(OGTT),计算其体重指数(BMI)、血糖曲线下面积(AUC glu)和胰岛素曲线下面积(AUC ins)、稳态模型评估胰岛素抵抗指数(HOMA-IR)、定量胰岛素敏感性指数(QUICKI)、Matsuda胰岛素敏感性指数(ISI)、稳态模型评估β细胞功能指数(HOMA-β)及胰岛素分泌敏感指数2(ISSI-2)。根据OGTT结果判定患者是糖代谢异常或糖代谢正常状态。采用两独立样本t检验、Mann-Whitney U检验或χ^(2)检验进行组间比较,采用二元logistic回归模型评估糖代谢异常和胰岛素抵抗(IR)的影响因素。结果共纳入44例GS患者和60例NFAI患者。与NFAI组相比,GS组患者糖代谢异常患病率更高[分别为25.00%(15/60)和63.64%(28/44),χ^(2)=15.625,P<0.001],AUC glu[分别为14.77(13.22,16.79)和16.63(14.53,20.50)mmol·h/L,Z=3.017,P=0.003]、AUC ins[分别为107.28(73.62,161.57)和156.55(111.76,234.50)mU·h/L,Z=3.296,P=0.001]均更大。在IR方面,与NFAI组相比,GS组患者的HOMA-IR升高[分别为1.64(1.27,2.32)和2.84(1.89,4.19),Z=4.257,P<0.001],而QUICKI[分别为0.35(0.34,0.37)和0.33(0.31,0.35),Z=-4.257,P<0.001]及ISI[分别为94.57(62.39,113.54)和46.55(33.39,83.98),Z=-4.514,P<0.001]均降低。在胰岛素分泌功能方面,与NFAI组相比,GS组患者的HOMA-β升高[分别为119.83(79.81,166.15)和157.62(110.25,252.38),Z=3.007,P=0.003],ISSI-2降低[分别为674.10(509.47,842.03)和588.38(335.11,699.66),Z=-2.704,P=0.007]。二元logistic回归分析结果显示,血镁(OR=0.62,95%CI 0.40~0.98,P=0.042)及血钾(OR=0.90,95%CI 0.80~0.99,P=0.046)均是GS患者发生糖代谢异常的独立影响因素;BMI(OR=1.61,95%CI 1.09~2.37,P=0.016ObjectiveTo investigate the factors that contribute to the glucose metabolism in patients with Gitelman syndrome(GS).MethodsThis was a case-control study.GS patients and non-functioning adrenal incidentaloma(NFAI)patients hospitalized at the Department of Endocrinology of the First Medical Center in Chinese PLA General Hospital from January 2013 to September 2023 were recruited.Fasting blood insulin,fasting plasma glucose,plasma potassium,plasma magnesium,height,and weight of these patients were collected,and an oral glucose tolerance test(OGTT)was performed.Body mass index(BMI),area under the curve of glucose(AUC glu),area under the curve of insulin(AUC ins),homeostasis model assessment of insulin resistance(HOMA-IR),quantitative insulin sensitivity check index(QUICKI),Matsuda insulin sensitivity index(ISI),homeostasis model assessmentβcell function(HOMA-β)and insulin secretion-sensitivity index-2(ISSI-2)were calculated.GS individuals were assigned to normal and abnormal glucose metabolism groups based on OGTT results.Two independent samples t-test,Mann-Whitney U-test,orχ^(2)-test were used for comparisons between groups.Logistic regression model was used to analyze the risk factors for impaired glucose metabolism and insulin resistance(IR)in GS patients.ResultsA total of 44 patients with GS and 60 patients with NFAI were included in the study.Compared with NFAI patients,higher prevalence of impaired glucose metabolism[25.00%(15/60)vs.63.64%(28/44),χ^(2)=15.625,P<0.001],higher AUC glu[14.77(13.22,16.79)vs.16.63(14.53,20.50)mmol·h/L,Z=3.017,P=0.003]and AUC ins[107.28(73.62,161.57)vs.156.55(111.76,234.50)mU·h/L,Z=3.296,P=0.001]were present in GS patients.Compared with NFAI patients,patients with GS showed higher HOMA-IR[1.64(1.27,2.32)vs.2.84(1.89,4.19),Z=4.257,P<0.001],lower QUICKI[0.35(0.34,0.37)vs.0.33(0.31,0.35),Z=-4.257,P<0.001]and lower Matsuda ISI[94.57(62.39,113.54)vs.46.55(33.39,83.98),Z=-4.514,P<0.001].Compared with NFAI patients,HOMA-β[119.83(79.81,166.15)vs.157.62(110.25,252.38),Z=3.007,P=0.003]
关 键 词:GITELMAN综合征 糖代谢异常 低镁血症 低钾血症 体重指数
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